Acta Anaesthesiol Taiwan 2009;47(4):212215

C ASE R EPORT

Recurrent Attacks of Post-intubation Right

Upper Lobe Atelectasis
Kyung Yeon Yoo1*, Seok Jai Kim1, Cheol Won Jeong1, Seong Tae Jeong1,
Yun Hyeun Kim2, Jong Un Lee3
1

Department of Anesthesiology and Pain Medicine, Chonnam National University Medical School,
Gwangju, South Korea.
2
Department of Radiology, Chonnam National University Medical School, Gwangju, South Korea.
3
Department of Physiology, Chonnam National University Medical School, Gwangju, South Korea.

Received: Jun 9, 2008

Revised: Dec 19, 2008
Accepted: Dec 24, 2008
KEY WORDS:
anesthesia, general;
propofol;
pulmonary atelectasis

A 22-year-old woman with no history of asthma developed an acute recurrent attack

of severe bronchoconstriction and right upper lobe atelectasis immediately after
laryngoscopy and endotracheal intubation. The first attack had taken place 2 months
earlier under identical circumstances. Induction of anesthesia for tracheal intubation was achieved using propofol, fentanyl, and rocuronium. Bronchial obstruction
and bronchial intubation were excluded by bronchoscopy. The atelectasis was quickly
resolved with mechanical ventilation and spasmolytic treatment on both occasions.
The surgical procedure could proceed soon after resolution of the atelectasis.

1. Introduction

2. Case Report

Major lung collapse secondary to inadvertent bronchial intubation1 or intrabronchial obstruction24

has been sporadically reported. Case reports on
lung collapse associated with acute reflex bronchoconstriction in the absence of intrabronchial
obstruction during induction of anesthesia are very
rare.57 We report herein a case of a seeming
healthy young female who twice developed severe
bronchoconstriction, with resultant acute collapse
of the right upper lobe (RUL) immediately after
induction of anesthesia in the operating room. The
first attack had taken place 2 months earlier in
identical circumstances.

A 22-year-old, 77-kg, 168-cm woman with a history of

hypertension for 8 years and cigarette smoking (< 1
pack/day) for 6 years was scheduled for extracranialintracranial arterial bypass for moyamoya disease.
Four months before this admission the patient had
undergone laparoscopic cholecystectomy smoothly
under general anesthesia with sevoflurane-50% nitrous oxide (N2O) in oxygen. Current medication
included irbesartan (300 mg daily) and triflusal
(300 mg 3 times daily). There was no history of
asthma, drug allergies, or pulmonary diseases. The
patient denied any bronchitic or upper respiratory
symptoms (e.g., coughing or phlegm production).

*Corresponding author. Department of Anesthesiology and Pain Medicine, Chonnam National University Medical School,
8 Hak-dong, Gwangju 501-190, South Korea.
E-mail: kyyoo@jnu.ac.kr
2009 Taiwan Society of Anesthesiologists

Acute alveolar collapse after anesthetic induction

213

Laboratory data (including complete blood count

and urinalysis) were within normal limits. Physical
examination, including heart and lung auscultation, revealed no evident acute or chronic disease.
Preoperative blood pressure was 132/82 mmHg,
heart rate was 76 beats/min, respiratory rate was
13 breaths/min, and oral temperature was 36.8C.
The patient was premedicated with midazolam
7.5 mg orally 60 minutes before induction of
anesthesia.
After insertion of an intravenous cannula and
placement of routine intraoperative monitoring
devices (including an electrocardiogram, invasive
blood pressure monitor, and pulse oximeter), anesthesia was induced with target-controlled infusion
of propofol with a target of 4 g/mL (Astra-Zeneca,
Macclesfield, UK), fentanyl 1.5 g/kg and rocuronium
1.5 mg/kg. Three minutes after induction, the trachea was easily intubated with a 7.0-mm endotracheal tube, which was secured between the lips at
the 22-cm mark, and the patient was ventilated
with 50% N2O in oxygen. Immediately following intubation, auscultation of the chest revealed bilateral
expiratory wheezing, louder on the left than on the
right, suggestive of bronchospasm. The peak inspiratory pressure then increased up to 3545 cmH2O,
and the tidal volume decreased to less than 200 mL
within 10 minutes of initiation of mechanical ventilation. N2O was discontinued, but her percutaneous hemoglobin oxygen saturation decreased to
92% while breathing 100% oxygen. Chest radiography taken at this juncture revealed RUL atelectasis
(Figure 1A). The tip of the tracheal tube was 2.5 cm
above the carina. The bronchospasm was treated
successfully with aerosolized albuterol, methylprednisolone 125 mg intravenously, and an aminophylline infusion at 20 g/kg/min, and flexible
fiberoptic bronchoscopy showed that the trachea

and the right and left endobronchial system were

free of obstruction by mucous or foreign bodies.
The surgery was cancelled, and the residual
neuromuscular block was reversed with pyridostigmine 15 mg and glycopyrrolate 0.4 mg intravenously. Satisfactory percutaneous hemoglobin oxygen
saturation (9698%) could be maintained while
spontaneously breathing 100% oxygen without any
sign of respiratory distress. The endotracheal tube
was then removed and the patient was transported
to the recovery room where she stayed for 2 hours
before being returned to the ward. Subsequent
chest X-ray, taken immediately after arrival at the
recovery room, revealed full re-expansion of the
collapsed RUL. Chest auscultation revealed absence of wheezing, and the breathing sounds were
equal bilaterally. The patient had no respiratory
problems afterwards and was discharged from hospital 5 days later.
Two months later, the surgery for moyamoya
disease was rescheduled, because her symptoms
were aggravated with right arm monoparesis and
intermittent dysarthria setting in. Following institution of standard monitoring and preoxygenation,
anesthetic induction and tracheal intubation were
achieved using propofol, fentanyl, and rocuronium
followed by continuous infusion of propofol with a
target of 4 g/mL, as in the previous anesthesia. As
before, the patient developed generalized bronchospasm with wheezing rales over the entire lung
fields shortly after endotracheal intubation. The
peak inspiratory pressure increased up to 40 cmH2O
and tidal volume progressively decreased to 200 mL.
Chest radiography revealed RUL collapse with the
tip of the tracheal tube 3.0 cm above the carina
(Figure 1B). The bronchospasm was treated successfully with aerosolized albuterol, intravenous
methylprednisolone, aminophylline infusion, and

Figure 1 Chest radiograph immediately after endotracheal intubation showing collapse of the right upper lobe at
first (A) and second (B) attempts of anesthesia for surgery of moyamoya disease.

214
mechanical ventilation. Fiberoptic bronchoscopy
showed that the trachea and bronchial tree were
free from obstruction. The surgery was called off,
and the residual neuromuscular block was reversed.
The patient was transported to the recovery room,
and a follow-up chest X-ray revealed nothing of
note. Chest computed tomography taken 2 days
afterwards showed no anatomic anomalies of the
tracheobronchial tree (e.g., tracheal bronchus)8 or
extraluminal mass. Neither the methacholine and
histamine bronchial provocation test, nor the skin
test for propofol, fentanyl and rocuronium performed 3 days after the second episode of atelectasis showed positive findings.

3. Discussion
It is generally agreed that atelectasis is caused by
obstruction of a bronchus (either because of massive secretion, aspiration, encroachment of a foreign body or intrabronchial intubation) followed by
rapid absorption of the trapped alveolar gas. In our
case, however, right main and upper lobe bronchi
were free from obstruction on fiberoptic bronchoscopy. A stimulus that increases vagal tone is known
to play an important role in triggering bronchial
obstruction, resulting in reflex atelectasis, which
is characterized by fast onset, absence of intrabronchial obstruction, and signs of parasympathetic
stimulation.57 Mechanical stimulation of the laryngeal mucosa has been demonstrated to reflexively
enhance vagal activity, irritating the trachea and
bronchi and increasing total lung resistance.9 Acute
RUL atelectasis was likely to have been associated
with the vagally-induced airway reflex in our case,
as manifested by acute onset of bronchospasm in
the absence of intrabronchial obstruction.
Interestingly, the patient did not show any signs
of acute bronchoconstriction during anesthetic induction for laparoscopic cholecystectomy in the
previous surgery, performed 4 months before. At
that time, anesthesia was induced with thiopental
sodium 375 mg and succinylcholine 80 mg, and
maintained with sevoflurane 23% and 50% N2O in
oxygen and vecuronium, while the two consecutive anesthesias were induced with propofol, fentanyl and rocuronium.
Unlike thiopental, propofol may decrease respiratory resistance and hence could prevent bronchospasm resulting from airway instrumentation.10
Moreover, propofol has been demonstrated to
significantly inhibit vagally-induced bronchoconstriction.11 Nevertheless, propofol is responsible
for perioperative anaphylactic shock in France in
1.2% of cases.12 Previous investigators have documented that propofol could cause bronchospam.1315

K.Y. Yoo et al
Although exceedingly rare, allergic reactions to
fentanyl, IntralipidTM and rocuronium have also
been described.12,16 Thus, drug (propofol, fentanyl,
or rocuronium)-induced bronchospasm may have
played a role in inducing intraoperative respiratory
difficulties. However, the absence of a severe
hypotensive episode and generalized erythema at
the onset of the wheezing would argue against
drug-induced histamine release as a priming event
in our case. In addition, the patient did not show
any signs of adverse reactions immediately after the
intravenous administration of those drugs before
the intubation. Moreover, neither the methacholine
and histamine bronchial provocation test, nor the
skin test for propofol, fentanyl and rocuronium
performed a few days thereafter were positive.
A bronchospasm without anaphylactoid reaction
after propofol administration has been reported in
a patient with sick house syndrome.17 In this case,
the drug lymphocyte stimulation test showed a positive reaction against propofol although a skin test
was negative, suggesting that propofol could be
responsible for the bronchospasm during the induction of anesthesia. It is suggested that bronchial
hypersensitivity may trigger bronchospasm in response to a sensitizing drug. Angiotensin-converting
enzyme inhibitors have also been demonstrated to
enhance bronchial responsiveness especially in
smokers.1820 As our patient was a smoker taking
irbesartan, we could not rule out the possibility that
irbesartan could be responsible for enhancing the
bronchospasm induced by propofol.
Although the underlying mechanisms are unclear, most acute lobar collapses associated with
bronchospasm after anesthesia induction developed selectively in RUL.3,5,7 It has been postulated
that the relatively straight, right mainstem bronchus and an almost 90 take-off of the RUL bronchus
may create a favorable condition for the Bernoulli
effect around the opening of RUL bronchus.21
Sprung et al7 suggested that this effect should be conspicuous when the lungs are vigorously ventilated,
because of increased resistance (bronchospasm),
causing rapid laminar air flow to be preferentially
directed toward the right lower and middle lobes,
bypassing the RUL bronchus, quickly drawing gas
out of the RUL and causing acute lobar collapse.
It may be difficult to decide whether the scheduled surgery should be carried out or not if the
patient develops reflex atelectasis. The operation
for moyamoya disease may be of long duration, and
it requires tight control of arterial carbon dioxide
tension during surgery. Therefore, under such circumstances, we postponed the surgery for our patient. In most reported cases, however, the scheduled
surgeries proceeded uneventfully without recurrence or aggravation, since the atelectasis resolved

Acute alveolar collapse after anesthetic induction

within an hour.6,7 Therefore, it may be reasonable
to proceed with the operation soon after the atelectasis has resolved.
In conclusion, it is suggested that acute lobar
atelectasis with bronchospasm during induction of
anesthesia may recur in a patient who had developed it previously. However, this reflex atelectasis
could be readily treated with mechanical ventilation and bronchodilators. It appears logical to
proceed with the planned procedure soon after
resolution of the atelectasis.

215
9.

10.

11.

12.
13.
14.

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